This is a 4-phase, investigator initiated, multicenter study. Its major purpose is to study important unanswered questions concerning the pathogenesis of human atherosclerosis using modern pathobiological approaches. To accomplish this, autopsies on persons (15-35 yr) killed by trauma will be done under rigorously controlled protocols to supply specified tissue samples for standardized biochemical and morphologic studies. The morphometric and biochemical analysis will be performed at designated Central Laboratories; these are: histotechnique (Univ of Chicago), morphometry (Ohio State Univ), and lipid biochemistry (Louisiana State Univ, New Orleans). The study design and all of the statistical aspects of the common protocol sections of the study, including the analysis of a major portion of the data, will be accomplished in the Central Statistical and Data Analysis Laboratory in San Antonio. The Central Laboratory at LSU will organize the data on risk factors from each case and will do most of the analyses on the post-mortem samples of blood. In this application the role of the Ohio State Univ in specimen collection and the activity of the Morphometry Central Laboratory (MCL) are presented. The Ohio State Univ will contribute 125 sets of specimens per year to the multicenter study. The MCL will analyze over 100,000 microscopic and macroscopic images generated in the study. The MCL will produce tabular data (e.g., lesion thickness) and spatial data (e.g., probability-of-occurrence maps). Among the major questions being addressed using data from the morphometry center are: 1) Do some fatty streaks progress to fibrous plaques and, if so, can the morphological characteristics of a transitional lesion be defined? 2) What is the evolutionary patter of different lesion types with increasing age? 3) What are the morphometric changes associated with progression? 4) What are the incidence and morphologic features of insudative (gelatinous) lesions and does the probability-of-occurrence map for these correlate with that of subsequent proliferative disease? 5) What structural features of lesions can be correlated with specific risk factors? 6) Are there morphometric differences in lesion structure between sexes that can account for the well-known differences in clinical course? 7) Do atherosclerotic structural features or risk factors data for young people provide any insight into the decline of coronary heart disease in the United States?